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- W2051222996 abstract "N-type calcium channels play an important role in synaptic transmission and a drug that blocks these channels has become an important tool in controlling chronic pain. The development of new N-channel-targeted drugs is dependent on a better understanding of the gating of these channels and how that gating can be modulated. We have previously concluded that ω-conotoxin GVIA (GVIA) is a gating modifier that acts by destabilizing the N-channel open state. However, this conclusion was largely based on our modeling results and requires experimental support. Roscovitine, a tri-substituted purine, has been shown to stabilize the N-channel open state to slow gating charge relaxation, which provides a direct test of our hypothesis for GVIA-induced gating modification. We found that roscovitine could modulate gating current in the presence of GVIA, which shows that roscovitine can still affect the gating of the GVIA-bound N-channel. However, the magnitude of the roscovitine-induced slowing of Off-gating current was significantly reduced. In addition to confirming our hypothesis, our evidence supports an additional effect of GVIA to alter gating transitions between N-channel closed states. By strongly limiting access to the N-channel open state, GVIA analogs that selectively induce this modulation could provide the basis for the next generation drugs that treat chronic pain." @default.
- W2051222996 created "2016-06-24" @default.
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- W2051222996 date "2010-09-01" @default.
- W2051222996 modified "2023-09-24" @default.
- W2051222996 title "Interference between two modulators of N-type (CaV2.2) calcium channel gating demonstrates that ω-conotoxin GVIA disrupts open state gating" @default.
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- W2051222996 doi "https://doi.org/10.1016/j.bbamem.2010.05.004" @default.
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